Vaping, or electronic cigarette (ecig) use, is prevalent among pregnant women, although little is known about the effects of perinatal ecig use on cardiovascular health of the progeny (even when using nicotine-free e-liquid). Maternal toxicant inhalation may adversely affect vital conduit vessel development. We tested the hypothesis that perinatal exposure to maternal vaping would lead to a dose-dependent dysfunction that would persist into later life of offspring. Pregnant Sprague-Dawley rats were exposed to either nicotine-free (Ecig0) or nicotine-containing Ecig aerosol (18 mg/ml, Ecig18) starting on gestational day 2 and continued until pups were weaned (postnatal day 21). Pups were never directly exposed. Conduit artery function (stiffness and reactivity) and structure was assessed in 3- and 7-month old offspring. At 3-months, pulse wave velocity (PWV) in the ecig0 and ecig18 offspring were significantly higher than controls in both the 20-puff/day (6.6±2.1 and 4.8±1.3 vs. 3.2±0.7 m/s, respectively, p<0.05, mean ± SD) and as 60-puff/day exposure cohort (7.5 ± 2.8 and 7.5 ± 2.5 vs 3.2 ± 0.5 m/s, respectively, p<0.01). Wire myography revealed (range of 23-31%) impaired aortic relaxation in all ecig exposure groups (with or without nicotine). Incubation of vessels with TEMPOL or Febuxostat reversed the aortic dysfunction, implicating involvement of reactive oxygen species. Nearly identical changes and pattern was seen in vascular outcomes of 7-month old offspring. The take home message from this pre-clinical study is that maternal vaping during pregnancy, with or without nicotine, leads to maladaptations in vascular (aortic) development that persist into adult life of offspring.
Chronic stress increases the risk of developing cardiovascular disease potentially via endothelial dysfunction. Decreased bioavailability of the potent vasodilator nitric oxide (NO) describes a hallmark of endothelial dysfunction. Nitrite (NO2‐) reduces into active NO, providing an alternative pathway of NO restoration. The effect of nitrite supplementation on aortic endothelial function has yet to be determined in chronically stressed mice. We hypothesized that nitrite supplementation would rescue chronic stress‐attributed impairments in aortic endothelial function. Male and female C57Bl/6 mice at 18 weeks‐of‐age underwent an unpredictable chronic mild stress (UCMS; 5 days/week for 7 hrs/day) paradigm to elicit a chronically stressed phenotype. Control and stressed mice underwent 8 weeks of NO2‐ supplementation (50mg/L) within their drinking water. At 26 weeks, mice were euthanized, and the thoracic aortas were removed and positioned in a wire myograph chamber. To assess vessel health, the aortas were precontracted with U46619 (7.5x10‐9M) and exposed to increasing concentrations of methacholine (MCh; 10‐9M to 10‐5M) and sodium nitroprusside (SNP; 10‐9M to 10‐5M). Maximal aorta dilation to MCh was impaired in UCMS mice vs. controls (71±3% vs 87±1%; p<0.05). However, chronic NO2‐ supplementation prevented the impairment in aortic dilation with UCMS (83±2% vs 71±3%; p<0.05). Maximal aorta dilation to SNP was not affected by UCMS and or NO2‐ supplementation, with normal aortic smooth muscle dilation. In conclusion, these data suggest an impairment in aortic endothelial function due to chronic stress that is prevented with chronic NO2‐ supplementation.
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